2013 Fiscal Year Final Research Report
Inhibition mechanism of the amyloid beta induced-cell death by komatsuna seed extracts: Challenge to Alzheimer's disease
| Project/Area Number |
24650494
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| Research Category |
Grant-in-Aid for Challenging Exploratory Research
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| Allocation Type | Single-year Grants |
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| Research Field |
Eating habits, studies on eating habits
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| Research Institution | Aichi Prefectural University |
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Principal Investigator |
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| Research Collaborator |
OKADA Mizue 中部学院大学, Yms Laboratory, 非常勤講師
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| Project Period (FY) |
2012-04-01 – 2014-03-31
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| Keywords | コマツナ種子 / アミロイドβ / 海馬神経細胞 / アルツハイマー型認知症 / インスリン / グルコース / 細胞死 / 活性酸素 |
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| Outline of Final Research Achievements |
Alzheimer's disease is characterized by large deposits of amyloid beta (Abeta) peptide. Abeta is known to increase reactive oxygen species (ROS) production in neurons, leading to cell death. In this study, we investigated the effects of komatsuna seed extracts (KSE) on Abeta (1-42)-induced neurotoxicity and on the regulation of cell death processing in hippocampus neurons (HN).
RESULTS: No bands of Abeta were recognized in Komatsuna by electrophoresis. In addition, Abeta modified by KSE did not bind to the insulin (Ins) receptor. In other words, promotion of the Ins uptake was seen. KSE showed enhancement of cell survival, compared to that of the control level, amounting to a 100% blockade of Abeta-induced cell death. Furthermore, intracellular ROS accumulation resulting from Abeta treatment was reduced when cells were treated with KSE. KSE improves glucose uptake by Abeta in HN. CONCLUSION: From these results, we suggest that KSE offers protection against Abeta-mediated cell death.
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| Free Research Field |
総合領域
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